Abstract
Higher plants adapt to different light intensities by altering hypocotyl elongation, stomatal density, seed size, and flowering time. Despite the importance of this developmental plasticity, knowledge of the underlying genetic and molecular mechanisms modulating and coordinating responses to light intensity remains incomplete. Here, I report that in Arabidopsis the PEAPOD (PPD) repressors PPD1 and PPD2 prevent exaggerated responses to light intensity. Genetic and transcriptome analyses, of a ppd deletion mutant and a PPD1 overexpression genotype, were used to identify how PPD repressors modulate the light signalling network. A ppd1/ppd2 deletion mutant has elongated hypocotyls, elevated stomatal density, enlarged seed, and delayed flowering, whereas overexpression of PPD1 results in the reverse. Transcription of both PPD1 and PPD2, upregulated in low light and downregulated in higher light, is activated by PHYTOCHROME INTERACTING FACTOR 4. I found PPDs modulate light signalling by negative regulation of SUPPRESSOR OF phyA-105 (SPA1) transcription. Whereas PPDs coordinate many of the responses to light intensity - hypocotyl elongation, flowering time, and stomatal density - by repression/de-repression of SPA1, PPD regulation of seed size occurs independent of SPA1. In conclusion PPD repressors modulate and coordinate developmental responses to light intensity by altering light signal transduction.